| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Original Research |
1 Department of Radiology, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku,
Tokyo 113-8603, Japan.
2 Department of First Internal Medicine, Nippon Medical School, Tokyo,
Japan.
Received March 26, 2004; accepted after revision October 15, 2004.
Address correspondence to Y. Amano
(yas-amano{at}nifty.com).
OBJECTIVE. The purpose of this study was to compare contrast-enhanced MRI with dual-radionuclide SPECT for the detection of myocardial damage associated with hypertrophic cardiomyopathy.
SUBJECTS AND METHODS. Twenty-three patients with hypertrophic cardiomyopathy were examined. Delayed hyperenhancement of the damaged myocardium was observed using contrast-enhanced MRI, and regional wall thickness and left ventricular ejection fraction were measured using cine balanced steady-state free precession MRI. Dual-radionuclide SPECT using technetium-99m sestamibi and iodine-123 15-(p-iodophenyl)-3-(R,S)-methylpentadecanoic acid (BMIPP) was performed at rest. In the abnormal myocardial segments, agreement between the contrast-enhanced MRI and 123I BMIPP SPECT was assessed. The relationships between the regional and global cardiac abnormalities and the delayed hyperenhancement on MRI and decreased uptake of 123I BMIPP were also evaluated.
RESULTS. In 368 left ventricular segments, 57 segments showed
delayed hyperenhancement on MRI, 43 segments showed decreased uptake of
123I BMIPP, and seven showed decreased uptake of 99mTc
sestamibi. The delayed hyperenhancement and decreased uptake of
123I BMIPP were frequently observed in the interventricular septal
wall (p < 0.0001); however, the agreement between the methods in
detecting myocardial abnormalities was fair (
= 0.38). The abnormal
septal walls were significantly thicker than those without apparent
abnormalities (p = 0.031). There was an inverse correlation between
the number of enhancing segments and the ejection fraction (r =
–0.53).
CONCLUSION. In hypertrophic cardiomyopathy, contrast-enhanced MRI was valuable for the detection of extensive myocardial damage.
Hypertrophic cardiomyopathy is characterized by abnormal thickening of the myocardium of the left ventricle in the absence of other cardiovascular diseases including hypertension, metabolic disorders, valvular diseases, myocardial infections, or tumors [1–3]. The cause of hypertrophic cardiomyopathy is complex, and the disease results from several genetic abnormalities and environmental factors [2]. Nonetheless, some features commonly occur in hypertrophic cardiomyopathy. They include a decreased coronary flow reserve, the frequent involvement of the interventricular septal wall, and impairments in myocardial compliance and global cardiac function [1, 2, 4, 5]. In hypertrophic cardiomyopathy, the assessment of myocardial damage, using various imaging techniques, is important for determining the clinical prognosis and for the selection of treatment regimens [6–10]. In the most serious hypertrophic cardiomyopathy cases, a decrease in perfusion, serious myocardial hypertrophy, and myocardial fibrosis are related to chest pain, syncope, and cardiac arrest. Therapy in these patients often requires implantation of a cardiac defibrillator, transluminal alcohol septal ablation, or a septal myomectomy.
In hypertrophic cardiomyopathy, MRI is useful for examining cardiac wall thickness and motion, left ventricular ejection fraction, and gradients in the left ventricular outflow tract [4, 5, 9–11]. The advantages of MRI include an unlimited field of view, high reproducibility, and the ability to estimate perfusion and coronary flow reserves. In recent animal and clinical studies, contrast-enhanced inversion recovery gradient-echo MRI showed delayed hyperenhancement of the myocardium in regions of myocardial scarring and fibrosis [9, 11, 12]. The delayed hyperenhancement, together with a decreased left ventricular ejection fraction, was consistent with the presence of serious hypertrophy and hypokinesis within the enhanced region of the myocardium [9, 11].
|
|
Two previous SPECT studies have shown that the abnormal washout of 99mTc tetrofosmin or 123I MIBG and the reduction of 123I BMIPP uptake correlate with measurements of the regional wall thickness and the mass of the left ventricle made from MRI images [15, 16]. However, contrast-enhanced MRI was not used in these studies.
In the present investigation, we assessed the ability of contrast-enhanced MRI and dual-radionuclide SPECT, using 99mTc sestamibi and 123I BMIPP, to detect the myocardial abnormalities associated with hypertrophic cardiomyopathy. We also investigated the relationship between delayed hyperenhancement as shown on MRI and the abnormalities of fatty acid metabolism as detected on 123I BMIPP SPECT, and the relationship between regional or global cardiac function and the number of abnormal ventricular segments observed on contrast-enhanced MRI or 123I BMIPP SPECT.
Subjects and Methods
Patient Selection
Twenty-three patients with hypertrophic cardiomyopathy (eight men and 15
women; mean age, 57.4 years; age range, 24–80 years) were prospectively
recruited to undergo MRI and SPECT examinations. The imaging studies were
approved by our institution, and informed consent was given by each subject.
The mean interval between the two studies was 10.0 days (SD, 9.5 days; range,
0–21 days). The diagnosis of hypertrophic cardiomyopathy was based on
the echocardiographic visualization of a hypertrophied, nondilated left
ventricle in the absence of another cardiovascular and systemic disease as
shown by echocardiography, X-ray coronary angiography, or SPECT
[1,
2]. Echocardiographic findings
showed that all patients had the septal hypertrophy. Six patients had an
apparent family history of hypertrophic cardiomyopathy. In 21 of the 23
patients, a diagnosis of hypertrophic obstructive cardiomyopathy was based on
clinical symptoms, a left ventricular outflow tract stenosis during systole,
and a left ventricular outflow tract gradient higher than 40 mm Hg.
Hypertrophic cardiomyopathy in the dilated phase was suspected in two patients
with the history of hypertrophic cardiomyopathy, left ventricular ejection
fraction below 50% (23.1% and 48.8%, respectively), and mild dilatation of the
right or left ventricular chambers.
MRI
All MR examinations were performed with breath-holding and used a 1.5-T
imager (Signa CVi, GE Healthcare) with a maximum gradient strength of 40 mT/m
and slew rate of 150 mT/m/msec. The phased-array cardiac multicoil, which
consisted of four channels, was used for signal reception. After three-plane
localizations and transverse fast spin-echo imaging, cine segmented balanced
steady-state free precession imaging (SSFP) was performed in the long- and
short-axes views using the following parameters
[17]: TR
range/TEeff, 4.2–4.8/1.7; flip angle, 60°; views per
segment, 16–24; cardiac phases after view sharing, 14–20; receiver
bandwidth, 125 kHz; imaging matrix, 256 x 128; field of view, 32 x
32 cm; slice thickness, 8–10 mm; and gap, 0–2 mm. Cardiac-gated
contrast-enhanced inversion recovery segmented fast gradient-echo imaging was
also performed in the short-axis view
[18]. The typical imaging
parameters were as follows: TR/TE, 5.5/1.4; inversion time, 250 msec; flip
angle, 20°; views per segment, 16; and receiver bandwidth, 31.3 kHz. The
inversion time of 250 msec was determined based on previous reports
[11,
19]. The image matrix and
section thickness in the contrast-enhanced images were identical to those of
the balanced SSFP images. Contrast-enhanced imaging, which was performed to
assess the delayed hyperenhancement of the myocardium, started 10 min after
the IV administration (0.15 mmol/kg) of gadolinium (gadodiamide hydrate
[Omniscan, Nycomed Amersham]).
|
|
|
|
|
|
Imaging Analysis
The left ventricular myocardium was divided into 16 segments according to
the American Heart Association statement
[21]. After getting the
consensus about this segmentation, two observers interpreted dual SPECT or
contrast-enhanced MR images independently. One observer, who was blinded to
the results of MRI, graded the SPECT images for the uptake of 99mTc
sestamibi and 123I BMIPP (normal, mild decrease, moderate or severe
decrease) [20]. Another
observer interpreted all MRI data without knowing the results of the
dual-radionuclide SPECT studies and visually assessed the presence of delayed
hyperenhancement, wall thickness at end-diastole and at end-systole,
percentage of septal wall thickening in systole, and left ventricular ejection
fraction. Corresponding to the grade of the reduction in the 123I
BMIPP uptake, the severity of the delayed hyperenhancement was graded on the
basis of the transmural extent as none, less than 50%, or 50% or greater
[22].
The number of segments that showed delayed hyperenhancement and reduced uptake of 99mTc sestamibi and 123I BMIPP was evaluated. A chi-square test was used to determine whether on the contrast-enhanced MR images and 123I BMIPP SPECT images, the interventricular septal wall (i.e., segments 2, 3, 8, 9, and 14) was involved more frequently than the other regions of the myocardium.
In the abnormal segments, the agreement between contrast-enhanced MRI and
123I BMIPP SPECT was assessed using kappa analysis. The level of
agreement ( value) was defined as follows: less than 0.21, poor;
0.21–0.40, fair; 0.41–0.60, moderate; 0.61–0.80,
substantial; and greater than 0.80, almost perfect.
The wall thickness at end-diastole and end-systole and the percentage systolic thickening of the septal wall were compared between normal segments and those with delayed hyperenhancement or reduction of 123I BMIPP uptake. An analysis of variance, subtested using Fisher's least squares difference, was used. In this analysis, segments 2 and 8 were evaluated in each of the 23 patients with asymmetric septal hypertrophy. These patients showed primary involvement of the segments and a smaller through-plane motion at the basal and midventricular levels of the myocardium than at the apical level [23].
Lastly, we assessed the correlation between left ventricular ejection fraction and the number of abnormal segments observed on contrast-enhanced MRI or 123I BMIPP SPECT. The left ventricular ejection fraction was estimated using short-axis balanced SSFP and Simpson's method. All statistical analyses were performed using statistical software (StatView, SAS International); a p value of less than 0.05 was defined as significant.
Results
A total of 368 segments were investigated in the 23 hypertrophic cardiomyopathy patients. In the contrast-enhanced MRI study, 57 segments (15.5%; 2.52 ± 2.87 segments per patient; range, 0–10 segments) showed delayed hyperenhancement. In the dual-radionuclide SPECT images, 43 segments (11.7%; 2.00 ± 2.55 segments per patient; range, 0–9 segments) and seven segments (1.9%) showed decreased uptake of 123I BMIPP and 99mTc sestamibi, respectively. Because only seven of the 368 segments showed reduction in 99mTc sestamibi uptake and all of these seven segments showed decreased uptake of 123I BMIPP, we excluded 99mTc sestamibi SPECT images from the subsequent statistical analyses.
Of the 57 segments with delayed hyperenhancement, 47 were located at the interventricular septal wall (p < 0.0001), and of the 43 segments with decreased uptake of 123I BMIPP, 26 were located at the septal wall (p < 0.0001). Thus, the septal wall is primarily involved in hypertrophic cardiomyopathy (Figs. 1A, 1B, 2A, 2B, 2C, 2D, 3A, 3B). In particular, segments 2 and 8 showed both delayed hyperenhancement (n = 21) and decreased uptake of 123I BMIPP (n = 18).
Agreement between the segments with delayed hyperenhancement and those with
decreased uptake of 123I BMIPP was fair ( = 0.38) (Fig.
1A,
1B). The kappa value was 0.23
when both delayed hyperenhancement (none; transmural extent, < 50%;
transmural extent, 
50%) and 123I BMIPP uptake (normal, mildly
decreased, moderately or severely decreased) were graded with a three-point
scoring system (Table 1).
|
In segments 2 and 8, the measurements of wall thickness at end-diastole and end-systole and percentage systolic thickening are summarized in Table 2. There were significant differences in the wall thickness at end-diastole (p = 0.031) and end-systole (p = 0.028) among the four types of segments 2 and 8. The segments that had both delayed hyperenhancement and a reduction in 123I BMIPP uptake were significantly thicker at end-diastole (p = 0.0064) and end-systole (p = 0.0060) than those that were normal on the contrast-enhanced MR images and 123I BMIPP SPECT images. The segments 2 and 8 that had delayed hyperenhancement and normal uptake of 123I BMIPP tended to be thicker at end-diastole than the normal segments (p = 0.05). However, an analysis of segments across all patients showed no significant difference in percentage systolic thickening (p = 0.393).
|
When the data for the two patients with hypertrophic cardiomyopathy in the dilated phase were excluded because of the hypokinesis and excessive decrease in the left ventricular ejection fraction values, the left ventricular ejection fraction ranged from 63.8 to 89.0 (mean, 78.26 ± 7.99 [SD]) and there was a significant inverse correlation between the number of hyperenhancing segments and the left ventricular ejection fraction (p = 0.012; r = –0.53) (Fig. 4). However, there was no correlation between the left ventricular ejection fraction and the number of segments showing decreased uptake of 123I BMIPP (p = 0.109).
|
In the abnormal myocardial segments, there was fair agreement ( =
0.38) between the contrast-enhanced MR images and 123I BMIPP SPECT
images. In the 20 segments showing decreased uptake of 123I BMIPP
with no delayed hyperenhancement, the fatty acid metabolism impairment was
thought to precede the myocardial fibrosis and scarring. Conversely, 34
segments exhibited delayed hyperenhancement without decreased 123I
BMIPP uptake. Even when the severities of the delayed hyperenhancement and
reduction in 123I BMIPP uptake were considered, there was also only
fair agreement ( = 0.23) between the transmural extent of delayed
hyperenhancement and the degree of reduction in 123I BMIPP uptake.
These results suggest that there are some differences in the pathologic
processes associated with delayed hyperenhancement, including scarring, and
the fatty acid metabolism impairment. In addition, the lower in-plane spatial
resolution and the high attenuation in the hypertrophied myocardium in the
SPECT images might be responsible for the failure to detect an abnormality in
the 123I BMIPP SPECT studies, despite the delayed hyperenhancement
in the MRI observation.
The thickened septal wall was primarily enhanced on MRI and also exhibited impairment of fatty acid metabolism on 123I BMIPP SPECT. These findings are consistent with those of previously published studies [9–11, 13, 15]. The septal wall segments with delayed hyperenhancement and decreased uptake of 123I BMIPP were significantly thickened at end-diastole and end-systole compared with the segments having a normal appearance. Although not statistically significant, the hyperenhancing segments with normal uptake of 123I BMIPP showed a tendency toward a thicker septal wall at end-diastole.
This study showed an inverse correlation between the number of the enhancing segments and left ventricular ejection fraction when the two patients with hypertrophic cardiomyopathy at the dilated phase were excluded from the sample. On the other hand, the number of segments with a reduction in 123I BMIPP uptake was not associated with left ventricular ejection fraction. These findings indicate that as hypertrophic cardiomyopathy progresses, the delayed hyperenhancement of the myocardium may be associated with regional and global cardiac dysfunction, but is not necessarily associated with the reduced uptake of 123I BMIPP.
This investigation had several limitations. First, the contrast-enhanced MR images and dual-radionuclide SPECT images differed in the in-plane spatial resolution and slice thickness of the myocardial segments. The segmentation used in this study, however, has been standardized previously using several tomographic imaging techniques [21]. Second, quantitative assessments of the uptake of 99mTc sestamibi and 123I BMIPP were not performed because of the difficulty in estimating the degree of both the uptake of isotopes and delayed hyperenhancement in the hypertrophied myocardium. The inversion time of contrast-enhanced MRI could have easily affected the visualization of delayed hyperenhancement, although the myocardial signals were suppressed using an inversion time of 250 msec in our study population [24]. Third, SPECT was not performed during exercise or pharmacologic stress because our patients had chest pain during daily exercise. Because contrast-enhanced MRI was not performed during stress, the SPECT during exercise or pharmacologic stress could not be applied for a fair comparison. The stress-induced SPECT examination may reflect reduction in coronary flow reserve and moderate ischemia rather than myocardial damage such as fibrosis and reduced metabolism. In addition, our patients complained of chest pain during daily exercise, which indicates the possibility of cardiac events during a stress test.
In conclusion, the degree of agreement between contrast-enhanced MRI and dual-radionuclide SPECT was fair. The delayed hyperenhancement on MRI reflected regional and global cardiac abnormalities better than 123I BMIPP SPECT. Therefore, for the evaluation of patients with hypertrophic cardiomyopathy, we recommend that contrast-enhanced MRI should be performed to show the extent of myocardial damage even in patients exhibiting no abnormalities on a dual-radionuclide SPECT study.
References
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  M. W. Hansen and N. Merchant MRI of Hypertrophic Cardiomyopathy: Part I, MRI Appearances Am. J. Roentgenol., December 1, 2007; 189(6): 1335 - 1343. [Abstract] [Full Text] [PDF]
|
|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
